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</x-tab>December 12, 2005<br>
<br>
TO: Biology Majors<br>
FROM: H. Robert Horvitz, Professor of Biology<br>
<br>
I am writing to inform you
of the exciting Advanced Undergraduate Seminar courses being offering
by the Department of Biology for the Spring 2006 term. A
complete list of the courses, instructors, and brief course
descriptions are enclosed. The topics are highly varied and
encompass areas of genetics, biochemistry, molecular biology, cell
biology and human disease. A student can take any number of
these courses. The courses, which generally involve four to
eight students, are for 6 units, graded pass/fail, and meet two hours
each week. The focus is on reading and discussing the primary
research literature. Most courses have two short written
assignments. Some include field trips to MIT research
laboratories or to commercial sites using technologies discussed in
the courses. The level of each course will be tailored to the
students who enroll. Because of the small size of these courses,
we expect students not to drop these courses once they have begun.<br>
<br>
These courses offer a
number of special features: small class size, a high degree of
personal contact with the instructor, a focus on the primary research
literature, and an opportunity to discuss current problems in biology
interactively. I believe these courses greatly enrich an
undergraduate's experience. There are limited alternative
opportunities available to undergraduates to interact closely with
instructors who are experienced full-time researchers; to learn to
read, understand, and analyze primary research papers; and to engage
in the type of stimulating discussions and debates that characterize
how science is really done. Most advanced MIT undergraduates
(generally juniors and seniors) have been sufficiently exposed to the
basics of biology to be able to read the primary literature and
appreciate both methodologies and cutting-edge advances. These
courses have two goals: first, to expose students to the kind of
thinking that is central to contemporary biological research; and
second, to impart specific knowledge in particular areas of biology.
These courses are designed to be intellectually stimulating and also
to provide excellent preparation for a variety of future careers that
require an understanding both of what modern biology is and of how it
is done. Students who have taken Advanced Undergraduate Seminars
in the past (different specific courses, same general design) have
been enormously enthusiastic about their experiences.<br>
<br>
I am writing to you
before Registration Day this Spring to encourage you to consider
enrolling for one of these seminar courses. Please feel free to
contact any of the instructors to learn more about their courses.<br>
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<div><font face="Times" color="#000000"><u><b>SPRING 2005-2006<br>
<br>
<br>
<br>
</b></u><b>7.340 Molecular Mechanism of Aging<br>
</b>Instructors: Danica Chen (</font><font
face="Times New Roman" color="#000000">danicac@mit.edu</font><font
face="Times" color="#000000">, 2-4140; laboratory of Lenny
Guarente)<br>
<span
></span> Agnieszka
Czopik (</font><font face="Times New Roman"
color="#000000">czopik@mit.edu,</font><font face="Times"
color="#000000"> 3-3567; laboratory of Lenny Guarente)<br>
Spring 2006. Thursdays, 1-3 pm. Room 68-151.<br>
<br>
Aging is a degenerative process that results in decreased viability
and increased susceptibility to diseases. This course will focus on
molecules and molecular pathways that regulate the aging process, such
as the insulin-signaling pathway and members of the Sir2 gene family.
We will discuss the molecular mechanism of calorie restriction, the
only known dietary regimen that extends the lifespans of a variety of
organisms. Other topics will include the human premature aging
disorders Werner's Syndrome and Hutchinson-Gilford Progeria, the role
of oxidative damage and the mitochondria in aging, and the effects of
metabolism on aging. We will explore the reciprocal effects of aging
and immunity at the cellular and molecular levels and the ways these
effects may be relevant to human biology. The class will be concluded
with tours of a research laboratory at MIT and a biotech company both
focused on aging.</font></div>
<div><font face="Times" color="#000000"><br>
<br>
<br>
<br>
<b>7.342 The RNA Revolution<br>
</b>Instructors:<x-tab> </x-tab>Rickard Sandberg
(sandberg@mit.edu, 3-7039; laboratory of Chris Burge)<br>
<span
></span> <x-tab
> </x-tab>Michael Stadler
(stadler@mit.edu, 3-7039; laboratory of Chris Burge)<br>
Spring 2006. Thursdays, 3-5 pm. Room 68-151.<br>
<br>
Recent findings have revolutionized our view of the roles of RNA in
biology. For example, short non-coding RNAs (microRNAs and short
interfering RNAs) play key roles in development and cancer by
regulating gene expression. The biology of short non-coding RNAs and
their importance in these processes will be topics for this course. In
addition, the mechanism of alternative splicing explains in part how
humans can express 500,000 different proteins with only 25,000 genes.
Alternative splicing, the process by which exons are joined in
different combinations to generate multiple variants of a gene, is
estimated to affect about 75% of all human genes. We will discuss how
alternative splicing diversifies the human protein repertoire,
influences sex determination and courtship behavior in fruit flies and
when disrupted can cause diseases such as spinal muscular atrophy.
Attention will also be given to catalytic RNAs that act in the
ribosome during protein synthesis. In each session we will critically
evaluate both the experimental and the computational techniques used
in the primary literature to foster an understanding of their
strengths and limitations. This course will give you an overview of
the exciting newly emerging roles for RNA.<br>
<br>
<br>
<b> <br>
7.343 Takin' Out the Trash: Quality Control in Cellular
Processes<br>
</b>Instructors: Peter</font><font face="Times New Roman"
color="#000000"> Chien (pchien@mit.edu; laboratory of Tania Baker)<br>
<span
></span> Eric Spear
(espear@mit.edu; laboratory of Chris Kaiser</font><font face="Times"
color="#000000">)<br>
Spring 2006. Wednesdays, 3-5 pm. Room 68-151. <br>
<br>
Messenger RNAs are synthesized from a DNA blueprint, the proteins
resulting from these messages are produced using the complex machinery
of the ribosome, and finally these proteins must attain their proper
mature folded state. Although this process is extraordinarily
accurate, care must be taken by the cell to cope with the inevitable
mistakes that occur along this long and complicated pipeline. To
this end, the cell has evolved a broad range of mechanisms to ensure
the quality of the final protein product. For example,
improperly folded proteins are often recognized as aberrant and
subsequently degraded, relieving the cell of the potentially
detrimental effects of a non-functional and abnormal protein. In
this class, we will discuss some of the many mechanisms used for
cellular quality control. We will consider the stresses that can
generate such aberrant protein products and how the cell continuously
fights these challenges. The recognition of misfolded proteins
and how these proteins are targeted to the degradative machinery will
also be discussed. We will consider both prokaryotic and
eukaryotic quality control, drawing attention to the similarities
between these two systems as well as highlighting differences between
them. The importance of these quality control mechanisms will be
emphasized throughout the course by discussing a number of relevant
human diseases, including cystic fibrosis, Huntington's Disease, and
certain types of cancer.<br>
<br>
<br>
<br>
<br>
<b>7.344 Toxins, Antibiotics, Protein Engineering and the
Ribosome<br>
</b>Instructors: Caroline</font><font face="Times New Roman"
color="#000000"> Koehrer (koehrer@mit.edu, 3-1870; laboratory of
Uttam<br>
<span
></span
> <span
></span> RajBhandary)<br>
<span
></span> Mandana
Sassanfar (mandana@mit.edu, 452-4371</font><font face="Times"
color="#000000">; Education Office)<br>
Spring 2006. Tuesdays, 1-3 pm. Room 68-151.<br>
<br>
What do the lethal poison Ricin,<i> Diphtheria</i> toxin, and the
widely used antibiotic tetracycline have in common? They all inhibit
protein synthesis by targeting the cell's translation machinery. Why
is Ricin such a powerful toxin? How does it work? If<i> Diphtheria</i>
toxin and tetracycline also inhibit translation, why do they have such
different consequences? How does resistance to antibiotics like
tetracycline arise? In this course, we will explore the mechanisms of
action of toxins and antibiotics that specifically target components
of the translational apparatus leading to the disruption of protein
synthesis. We will discuss the roles of these antibiotics and toxins
in everyday medicine, the emergence and spread of drug resistance, and
how we might overcome this increasing problem by identifying new drug
targets and designing new drugs. We will also discuss how the detailed
understanding of the structure of the ribosome and the translation
machinery has led to new technologies in protein engineering and
promising applications for human therapy. </font></div>
<div><font face="Times" color="#000000"><b><br></b></font></div>
<div><font face="Times" color="#000000"><b><br>
7.346 How Abnormal Protein Folding Causes Alzheimer's,
Parkinson's, Mad Cow<br>
and Other
Neurodegenerative Diseases<br>
</b>Instructor: Atta</font><font face="Times New Roman"
color="#000000"> Ahmad (giftee6@mit.edu, 3-3707;
laboratory</font><font face="Times" color="#000000"> of Vernon
Ingram)<br>
Spring 2006. Thursdays, 11 am - 1 pm. Room 68-151.<br>
<br>
The cause of both Alzheimer's Disease (AD) and Parkinson's Disease
(PD) is abnormal deposition of proteins in brain cells. In addition,
there are 20 other neurological diseases caused by similar protein
deposition. Millions of people suffer from these diseases. The latest
research shows that these diseases arise as a consequence of a
specific series of molecular events. First, a protein assumes a
non-native sticky "misfolded state." Two or more such sticky
proteins associate together to generate a multi protein "oligomeric
state." These oligomers can associate with each other or can recruit
newly formed sticky proteins, thereby growing into bigger thread-like
structures called "amyloid fibrils." These fibrils can deposit
either inside or outside brain cells, disrupting normal biological
functions and resulting in neuronal cell death. Depending on the
region of the brain affected, this cell death leads to visible
symptoms, such as memory loss, loss of cognitive ability, abnormal
muscular movements, involuntary shaking and, in many cases, death. In
this course, we will discuss the processes that trigger protein
aggregation (such as, mutations and environmental effects) with an
emphasis on Alzheimer's Disease, Parkinson's Disease and Mad Cow
Disease. The methods used to study the processes of aggregation
(<i>e.g.</i>, fluorescence spectroscopy, circular dichroism, infrared
spectroscopy, transmission electron microscopy, confocal microscopy)
will be discussed. We will consider the consequences of the aberrant
proteins on cellular processes. We will also discuss potential targets
for intervening with these processes and approaches that could lead to
possible treatments for these disorders.<br>
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